Where the rubber hits the road

Plastics are an essential resource in modern society due to their versatility and durability. However, million of tons of plastics end up in landfills globally, where they break down into smaller-sized particles called micro- and nanoplastics (MNPs). A major source of MNPs in outdoor air is rubber abraded from vehicle tyres, mixing with road dust to form what are collectively referred to as tyre and road wear particles. Once airborne, these particles can be inhaled by humans, resulting in potential respiratory or immune-related perturbations. A major component of this thesis is a human volunteer study using a semi-controlled short-term exposure at three urban sites in Utrecht, The Netherlands, downwind from local traffic sources: an urban park (background), a highway with continuous driving traffic, and a stop-and-go traffic site. We assessed the mass of synthetic and natural rubber markers within particulate matter ≤10µm collected on-site for 4-hour periods (n = 23 days), using pyrolysis gas-chromatography mass-spectrometry (Chapter 2), and the concentrations of other (traffic-related) air pollutants. Overall, traffic-related MNP levels were relatively low compared to total PM10 levels, contributing on average 0.23% (max 1.23%), but were consistently higher (2–5-fold) at the traffic sites versus the park, with similar patterns for black carbon and brake-wear metals. Small groups of volunteers (n = 23) visited each measurement site once for 4 hours, while performing 80 minutes of intermittent exercise (Chapters 3 and 4). Venous blood was collected before each visit and at two post-exposure times (5.5 and 21.5 hours post-baseline) for white blood cell counts, 42 cytokines/chemokines (OLINK® panel), and activation/maturation markers on white blood cells. Immediately before and after each visit, lung function and respiratory symptoms were assessed. We observed positive, robust associations between an IQR increase in traffic-related MNPs and monocytes (7.1–9.3%) immediately after exposure, and the following morning, positive associations for total- and differential white blood cell counts, including monocytes (9.3–17.7%) and granulocytes (7.4–14.0%), independent of co-pollutants. No acute respiratory changes were observed. The following morning, plasma showed significant FDR-corrected downregulation of CXCL9 and IL18 (2.3–8.5%), and small negative associations with CD16 (-5%) and CD11b (-25.5%), though not independent of black carbon or brake-wear metals. These findings may indicate redistribution of circulating immune cells rather than classical inflammation, though this remains speculative. Using nationwide administrative data from Statistics Netherlands (CBS), we investigated whether individuals with higher long-term exposure to tyre and brake wear particles had an increased mortality risk from natural or specific causes, including non-malignant respiratory disease, lung cancer, cardiovascular disease, and neurological disorders. Our study population included ~9.6 million individuals aged 30 years or older, followed from 2013 to 2019, using cox-proportional hazard models adjusted for individual- and area-level covariates. Higher PM-TBW was associated with increased natural and cause-specific mortality, most consistently for non-malignant respiratory disease and neurological disorder, whereas cardiovascular mortality showed null associations. This dissertation demonstrates traffic-related MNPs constitute a measurable, biologically relevant component of traffic pollution, suggesting non-exhaust emissions warrant consideration alongside exhaust pollutants in air quality policy.